A systematic review of amino acid PET in assessing treatment response to temozolomide in glioma.

The response assessment in neuro-oncology (RANO) criteria have been the gold standard for monitoring treatment response in glioblastoma (GBM) and differentiating tumor progression from pseudoprogression. While the RANO criteria have played a key role in detecting early tumor progression, their ability to identify pseudoprogression is limited by post-treatment damage to the blood-brain barrier (BBB), which often leads to contrast enhancement on MRI and correlates poorly to tumor status. Amino acid positron emission tomography (AA PET) is a rapidly growing imaging modality in neuro-oncology. While contrast-enhanced MRI relies on leaky vascularity or a compromised BBB for delivery of contrast agents, amino acid tracers can cross the BBB, making AA PET particularly well-suited for monitoring treatment response and diagnosing pseudoprogression. The authors performed a systematic review of PubMed, MEDLINE, and Embase through December 2021 with the search terms "temozolomide" OR "Temodar," "glioma" OR "glioblastoma," "PET," and "amino acid." There were 19 studies meeting inclusion criteria. Thirteen studies utilized [18F]FET, five utilized [11C]MET, and one utilized both. All studies used static AA PET parameters to evaluate TMZ treatment in glioma patients, with nine using dynamic tracer parameters in addition. Throughout these studies, AA PET demonstrated utility in TMZ treatment monitoring and predicting patient survival.

Natural history of intracranial meningiomas.

We know that the extent of resection is the greatest predictor of long-term survival. However, the potential tradeoff for gross total resection in difficult locations is diminished quality of life. Benign subtotally resected or small incidentally discovered meningiomas may be followed clinically especially in the elderly. In addition, radiosurgery plays a role in the treatment of meningiomas as a primary treatment modality, or as a salvage therapy. Decisions regarding management should be made with an understanding of the natural history and rate of growth. In this chapter we review the known meningioma epidemiology as well as the growth patterns of meningiomas based upon location.

Mini-Pterional Craniotomy for Resection of Parasellar Meningiomas.

BACKGROUND: Surgical resection of parasellar meningiomas is a challenging operation that traditionally has been performed with a large pterional or orbitozygomatic craniotomy. In this study, we report patient outcomes and detail our surgical approach when resecting these tumors with a smaller, less invasive "mini-pterional" craniotomy. METHODS: We performed a retrospective review on all patients undergoing a mini-pterional craniotomy for resection of parasellar meningiomas from 2012 to 2016. We describe the technical aspects of the mini-pterional craniotomy and provide the outcomes of patients who received an operation with this approach. RESULTS: Twenty-four patients were treated with a mini-pterional craniotomy for resection of parasellar meningiomas. Median tumor volume was 6.2 cm3. Twenty-two of 24 (92%) patients had a World Health Organization grade I meningioma, and 2 of 24 (8%) patients had a World Health Organization grade II meningioma. Tumors were located at the medial sphenoid wing (60%), anterior clinoid (24%) and spheno-cavernous junction (12%). Nineteen of 24 (79%) patients had a Simpson Grade I resection and 5 of 24 (21%) a Simpson Grade IV resection. Median length of the operations was 242 minutes. Neurosurgical complications occurred in 2 patients who had a surgical-site infection and cerebrospinal fluid leak; one of these patients also developed postoperative hydrocephalus. In this series, no deaths, parenchymal contusions, or repeat operations occurred. CONCLUSIONS: The mini-pterional craniotomy can be used to resect parasellar meningiomas with good results and a low complication profile. This approach provides an efficacious method of resecting these tumors without sacrificing Simpson grade or patient safety.

Myelopathy Improvement Following Removal of Cervical Sublaminar Wiring.

Posterior cervical wiring has been used by spine surgeons in fixation procedures for patients with spinal instability. It is historically considered an effective method of treating cervical instability with a low risk of complications leading to neurological deterioration. We experienced a case of delayed neurological decline associated with myelopathy, lower extremity spasticity, and associated syringomyelia secondary to instrumentation failure and resultant sublaminar wire protrusion into the cervical spinal cord. In the present case, the construct was removed and the patient underwent a durotomy repair and a posterior fusion of cervical levels 1 and 2 via screw placement under image guidance with a subsequent functional improvement back to baseline. We report this case and review the literature on the complications associated with cervical wire fusion and the methods of minimizing these risks.

Primary Intracranial Sarcoma Presenting as Chronic Subdural Fluid Collections in a Child.

BACKGROUND: Chronic subdural hematoma in the pediatric population often results from trauma. Asymptomatic and benign-appearing subdural collections are generally managed conservatively without operative intervention. Primary intracranial sarcomas are uncommon entities. Diagnosis of sarcoma can be difficult because these lesions often manifest as apparent hematoma. CASE DESCRIPTION: Presented is the case of a primary intracranial mucoid spindle cell sarcoma that arose in a child with a history of benign-appearing bilateral subdural fluid collections in the setting of nonaccidental trauma. The patient was initially managed conservatively because her neurological examination result was normal and her subdural collections decreased in size on repeated imaging. The collections did not resolve completely. Years later, she exhibited weakness, seizure, and an increase in the size of her subdural fluid collection. Subdural drainage was attempted without significant effect. Cytologic assessment of fluid was negative for malignant cells. Magnetic resonance imaging revealed multiple enhancing masses along the subdural collection. The patient eventually underwent craniotomy in which a diagnosis of sarcoma was obtained. Pathological and radiographic findings as well as oncological management are reviewed. The authors also review the natural history and treatment of primary intracranial sarcoma in the pediatric population. CONCLUSIONS: Early contrasted magnetic resonance imaging should be obtained in patients with subdural fluid collections that appear asymmetric or do not resolve in the expected time course, despite having a normal neurologic examination result. Negative cytologic assessment does not exclude sarcoma diagnosis.

Identification of a region of rat chromosome 1 that impairs the myogenic response and autoregulation of cerebral blood flow in fawn-hooded hypertensive rats.

This study examined the effects of transfer of a 2.4-Mbp region of rat chromosome 1 (RNO1) from Brown Norway (BN) into fawn-hooded hypertensive (FHH) rats on autoregulation (AR) of cerebral blood flow (CBF) and the myogenic response of middle cerebral arteries (MCAs). AR of CBF was poor in FHH and FHH.1(BN) AR(-) congenic strains that excluded the critical 2.4-Mbp region. In contrast, AR was restored in FHH.1(BN) AR(+) congenic strains that included this region. The diameter of MCAs of FHH rats increased from 140 ± 14 to 157 ± 18 µm when transmural pressure was increased from 40 to 140 mmHg, but it decreased from 137 ± 5 to 94 ± 7 µm in FHH.1(BN) AR(+) congenic strains. Transient occlusion of MCAs reduced CBF by 80% in all strains. However, the hyperemic response following ischemia was significantly greater in FHH and AR(-) rats than that seen in AR(+) congenic strains (AR(-), 173 ± 11% vs. AR(+), 124 ± 5%). Infarct size and edema formation were also significantly greater in an AR(-) strain (38.6 ± 2.6 and 12.1 ± 2%) than in AR(+) congenic strains (27.6 ± 1.8 and 6.5 ± 0.9%). These results indicate that there is a gene in the 2.4-Mbp region of RNO1 that alters the development of myogenic tone in cerebral arteries. Transfer of this region from BN to FHH rats restores AR of CBF and vascular reactivity and reduces cerebral injury after transient occlusion and reperfusion of the MCA.